2015-Myofibrillogenesis regulator-1 attenuates hypoxia reoxygenation-induced injury by repairing microfilaments in neonatal rat cardiomyocytes.

2015-Myofibrillogenesis regulator-1 attenuates hypoxia reoxygenation-induced injury by repairing microfilaments in neonatal rat cardiomyocytes.

ID:40705854

大小:2.58 MB

页数:9页

时间:2019-08-06

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1、ExperimentalCellResearch337(2015)234–242ContentslistsavailableatScienceDirectExperimentalCellResearchjournalhomepage:www.elsevier.com/locate/yexcrResearchArticleMyofibrillogenesisregulator-1attenuateshypoxia/reoxygenation-inducedinjurybyrepairingmicrofilamentsinneonatalratca

2、rdiomyocytesnTianqiTao,XiaorengWang,MiLiu,XiuhuaLiuDepartmentofPathophysiology,ChinesePLAGeneralHospital,100853Beijing,ChinaarticleinfoabstractArticlehistory:Hypoxia/reoxygenation(H/R)injuryischaracterizedbymicrofilamentreorganizationincardiomyocytes.Received1March2015Previ

3、ousstudieshaveshownthatmyofibrillogenesisregulator-1(MR-1)isexpressedinthemyocardiumReceivedinrevisedformandpromotesactinorganizationincardiomyocytes.Thepurposeofthisstudywastoinvestigatetherole20May2015ofMR-1inattenuatinghypoxia/reoxygenationinjuryincardiomyocytesthroughpr

4、omotingrestorationAccepted30May2015ofthemicrofilament.Toaddressthisaim,anH/RmodelofculturedneonatalcardiomyocyteswasusedtoAvailableonline4June2015assessfilamentousactin(F-actin)andα-actininorganizationthroughimmunofluorescencemicroscopyKeywords:analysis.RT-PCRwasusedtodetectm

5、RNAlevelsofMR-1andmyosinregulatorylightchain-2(MLC-2).Hypoxia/reoxygenationWesternblotanalysiswasusedtodetectproteinlevelsofMR-1andfilamentousactin/globularactin(F-/CardiomyocyteG-actin)aswellasMLC-2andmyosinlightchainkinase(MLCK)phosphorylationandproteinexpression.Myofibril

6、logenesisregulator-1WealsoexploredtheeffectsofoverexpressingorknockingdownMR-1onH/RinjuryandtheMLCK/MicrofilamentMLC-2/F-actinpathway.WefoundthatH/RinducedcardiomyocyteinjuryanddisruptionofF-actinandα-actininwithadecreaseintheF-/G-actinratiocomparedwithcontrols.Comparedwith

7、theH/Rgroup,MR-1overexpressionattenuatedH/R-inducedinjuryanddisruptionofF-actinandα-actininincardio-myocyteswithanincreaseintheF-/G-actinratio.MR-1overexpressionalsoup-regulatedH/R-inducedMLCKandMLC-2phosphorylation.However,MR-1knockdownaggravatedH/Rinjurybyfurtherdis-rupt

8、ingF-actinandα-actinin,aswellasdecreasingtheF-/G-actinratio.MR-1knockdownalsodown-regulat

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